A case of Grave’ s disease complicated with thyrotoxic hepatic failure and thyrotoxic period paralysis.

wiem saafi; Abdelkarim Asma Ben; Abdallah Bouthaina Ben; Ghada Saad; Aya hammami; ameur wafa ben; Amel Maaroufi; Maha Kacem; Molka Chaeib; Hanen Jaziri; Yosra Hasni; Koussay Ach

doi:10.1530/endoabs.73.AEP771

Introduction

Grave’s disease is an autoimmune thyroid disorder. It is the most frequent cause of hyperthyroidism with variable manifestations. When not recognized in time and not adequately treated, Graves’ disease poses serious risks and can have severe complications.

Observation

A 63-year-old female was admitted to the endocrinology department for severe thyrotoxicosis. She was diagnosed in 2011 with Grave’s disease medically treated using Benzylthioluracil. She has been in remission since 2015. She had a SARS-CoV-2 infection three months ago. Two months before her admission, the patient presented vomiting and diarrhea with a weight loss and jaundice. The physical examination revealed no signs of thyroid eye disease and no goiter with a regular pulse rate of 120 beats and a normal blood pressure. The patient had no hepatomegaly. she was alert and oriented with 1/5 strength in the lower extremities with no sensory deficits. Laboratory investigations confirmed the diagnosis of hyperthyroidism showing high serum free T4 (7.7 ng/dl) and low serum thyroid-stimulating hormone (TSH <0.001 IU/l). Sodium 140 mmol/l, potassium 2.4 mmol/l. Hepatic function tests revealed cytolysis cholestasis and hepatic failure: total bilirubin 519 µmol/l, direct bilirubin 300 µmol/l, alkaline phosphatase 84 U/l, gamma-glutamyl transferase 22U/l, aspartate aminotransferase 249 U/l, and alanine aminotransferase 174 U/l; prothrombin time 40% a normal factor V level. Viral serologies and investigations for other autoimmune disease and hepatic disease antinuclear antibodies, anti-smooth muscle antibodies, anti-liver kidney microsomal antibodies and anti-mitochondrial antibodies were negative and abdominal imaging did not show hepatic lesions. The diagnosis of thyrotoxic hepatitis associated with a thyrotoxic periodic paralysis was retained. The patient was treated with corticosteroids and a high dose of Benzylthioluracil, and a potassium correction. Ten days after treatment initiation, the thyroid function was normal with regression of cytolysis and cholestasis. The patient regained normal strength, and she received radioiodine therapy.

Discussion

In this case, we report two different complications of Grave’s disease. Liver injury caused by thyrotoxicosis is relatively common and can be conveniently divided into hepatitis or cholestatic types. It represents a real problem since it can limit the use of antithyroid drugs and prolong the state of hyperthyroidism, exposing the patient to more severe complications. As for thyrotoxic period paralysis, it is a severe and rare complication of hyperthyroidism. When not recognized, it can lead to respiratory failure and possibly death.

Endocrine Abstracts

AEP771